Dynamics of the antibody-T.cruzicompetition during Chagas infection: Prognostic relevance of intracellular replication

Abstract

A recently proposed model for the competitive parasite-antibody interactions in Chagas disease is extended by separately describing the parasitic intracellular and extracellular phases. The model solutions faithfully reproduce available population data and yield predictions for parasite-induced cardiac cell damage.

Why does GM1 induce a potent beneficial response to experimental Chagas disease?

“…We remark that a higher in vitro value of N r is not surprising because of the better feeding of (and weaker constraints on) cells in a monolayer culture. Although we know of no direct measurements of the penetration time, we can compare ͑0.17 dpi −1 ͒ with our previous results for other mice/parasite strains (Sibona et al, 2005). For instance, for BALBc/Tulahuen we obtained = 0.33 dpi −1 .…”

“…The parameters ⍀ and N r can be related to the mean amastigote duplication time by considering a Malthusian model for the amastigote replication dynamics (Sibona et al, 2005;Sibona et al, 2007). A simple calculation yields…”

“…Since blood parasites are the infective forms, antibodies become a central part of the host defense against T. cruzi. Our basic model is built upon the following assumptions: These assumptions are embodied in a set of first-order equations that describe the evolution of the various populations (Sibona et al, 2005;Sibona et al, 2007). If N antibody species are present, the equation for the total number of circulating trypomastigotes, n͑t͒, is dn͑t͒ dt…”

“…It also reproduces experimental data and permits us to estimate the damage generated by direct parasitic action (Sibona et al, 2007). This model was used to investigate diverse situations of interest, such as the action of parasite-released decoys, the influence of immune reaction delays, and the effects of an increase in the antibody efficiency (Sibona et al, 2005). Since the mechanisms of GM1 action have not yet been elucidated, we now challenged our model with data from the experiments in Cossy Isasi et al (1999), in order to uncover clues to their nature.…”

A MATHEMATICAL MODEL TO ASSESS THE IMMUNE RESPONSE AGAINSTTRYPANOSOMA CRUZIINFECTION

“…The aim of this paper is the development of a mathematical model to assess the role played by humoral and cellular immune responses to control T. cruzi infection. Isasi et al 9 and Sibona et al 10 analyzed mathematical models taking into account the parasite population and the diversity of antibodies, while Velasco-Hernandez and Perez-Chavela analyzed a model for the cellular immune response to T. cruzi. 11 The paper is structured as follows.…”